Cardiovascular disease accounts for nearly fifty percent of deaths in both the developed world and in developing countries. Indeed, the risk of dying from heart disease is greater than the risk from AIDS and all forms of cancer combined. Worldwide, cardiovascular disease causes 12 million deaths each year. It is the leading cause of death in the U.S., killing some 950,000 people each year. It also accounts for a significant amount of disability and diminished quality of life. Some 60 million people in the U.S. alone have some form of heart disease. Therefore, a great need exists for the advancement of devices and procedures to cure, treat, and correct a wide variety of forms of heart disease.
Normal heart function primarily relies upon the proper function of each of the four valves of the heart, which pass blood through the four chambers of the heart. The four chambers of the heart include the right atrium and left atrium, the upper chambers, and the right ventricle and left ventricle, the lower chambers. The four valves, controlling blood flow in the chambers, include the tricuspid, mitral, pulmonary, and aortic valves. Heart valves are complex structures that rely on the interaction of many components to open and close the valve. More particularly, each of the four valves of the heart have cusps or leaflets, comprised of fibrous tissue, which attach to the walls of the heart and aid in controlling the flow of blood through the valves. The mitral valve has two leaflets and the tricuspid valve has three leaflets. The aortic and pulmonary valves have three leaflets that are more aptly termed “cusps,” stemming from their half moon shape.
The cardiac cycle involves the pumping and distribution of both oxygenated and deoxygenated blood within the four chambers. In systole, or the rhythmic contraction of the heart cycle, oxygenated blood, enriched by the lungs, enters the heart into the left atrium or left upper chamber. During diastole, or the resting phase of heart cycle, the left atrial pressure exceeds the left ventricle pressure; thus, oxygenated blood flows through the mitral valve, a one way inflow valve, into the left ventricle. The contraction of the left ventricle pumps the oxygenated blood through the aortic valve, into the aorta, and is passed on to the body. When the left ventricle contracts in systole, the mitral valve closes and the oxygenated blood passes into the aorta. Deoxygenated blood returns from the body via the right atrium. This deoxygenated blood flows through the tricuspid valve into the right ventricle. When the right ventricle contracts, the tricuspid valve closes and the deoxygenated blood is pumped through the pulmonary valve. Deoxygenated blood is directed to the pulmonary vascular bed for oxygenation, and the cardiac cycle repeats itself.
The performance of the cardiac cycle by the various components of the heart is a complex and intricate process. Deficiency in one of the components of the heart or deficiency in the performance of the cardiac cycle most often leads to one or more of the numerous different types of heart disease. One of the most prevalent heart disease conditions is mitral valve regurgitation. Mitral valve regurgitation has many levels of severity. After 55 years of age, some degree of mitral regurgitation is found in almost 20% of men and women who have an echocardiogram. Mitral valve regurgitation, or mitral regurgitation, is a condition in which the mitral valve does not close tightly, thereby allowing blood to flow backward in your heart.
FIG. 1 provides an illustration of a normal mitral valve 101. As shown in FIG. 1, the mitral valve 101 includes a mitral annulus 105, an anterior mitral leaflet 110 and a posterior mitral leaflet 115, the chordae tendineae 120, and the medial and lateral papillary muscles, 135 and 140. The term mitral annulus refers to the elliptical region of the valve leaflet attachment contiguous with the base of the left atrium. The mitral annulus 105 is composed of an anterior mitral annulus 125 and a posterior mitral annulus 120. The mitral annulus 105 is saddle shaped with the basal portions of the saddle located medially and laterally. Attached to the anterior mitral annulus 125 is the anterior mitral leaflet 110 and attached to the posterior mitral annulus 130 is the posterior mitral leaflet 115. The regions where the anterior mitral leaflet 110 and the posterior mitral leaflet 115 meet are termed the lateral commissure 145 and the medial commissure 150.
In a normal mitral valve, when the atrial pressure exceeds the ventricular pressure, the valve leaflets open into the ventricle. When the ventricle pressure increases, the leaflets meet and close, covering the area of the valve annulus. Therefore, in the diagram shown in FIG. 1, anterior mitral leaflet 110 and the posterior mitral leaflet 115 will open during diastole to allow blood to flow through the mitral valve 101. Conversely, the anterior mitral leaflet 110 and the posterior mitral leaflet 115 will overlap and close the mitral valve 101 to prevent regurgitation, or backflow of blood, into the left atrium during systole.
The function of an atrioventricular valve, like the mitral valve, involves the complex interaction of numerous components, including the leaflets, chordae tendineae, and the papillary muscles. If one of the components or functions of the complicated interaction fails, then mitral valve regurgitation can result. For example, excess leaflet tissue, inadequate leaflet tissue, or restricted motion of the leaflets can lead to mitral regurgitation. Prolonged and/or severe mitral valve regurgitation can result in an overworked left ventricle. Overworking the left ventricle can lead to left ventricle enlargement and dysfunction resulting in heart failure. Mitral valve regurgitation is a progressive condition that, if not corrected, can be fatal.
Surgical treatment of ischemic mitral regurgitation (IMR) continues to be hampered by suboptimal clinical results and excessive long-term mortality. Mitral valve repair is preferred to valve replacement for most causes of mitral regurgitation but remains challenging for patients with IMR. Currently, small ring annuloplasty represents the standard mitral repair technique for IMR. Newer reparative techniques have been proposed to address this challenging disease.
U.S. Pat. No. 7,087,064 to Hyde (“'064 patent”) describes a conventional technique for the treatment of mitral valve regurgitation, involving the use of a percutaneously deployable ligament. FIG. 2 provides an illustration of the ligatures of the '064 patent deployed in a mitral valve. As described in the '064 patent, the ligatures are percutaneously deployed, through the blood vessels, veins, or arteries into the heart. After deployment, the ligatures are then attached to the fibrous ring of the mitral valve on opposite sides of the mitral valve. The placement of ligatures that are smaller in diameter than the mitral valve annulus serves to constrict, reshape or reduce the circumference of the mitral valve.
As an alternative to the passive ligature method of the '064 patent, an experimental technique of Septal-Lateral Annular Cinching (SLAC) with a central transannular suture has shown some positive results. SLAC presents many potential advantages in comparison to more conventional techniques of treating heart dysfunctions and avoiding congestive heart failure. Conventional approaches and devices of treatment of the mitral valve have often resulted in a modification of the normal function of the valve. For example, some techniques treat mitral valve regurgitation by freezing the posterior leaflet of the valve, thus converting the bi-leaflet valve into a uni-leaflet valve. In a non-limiting example, ring annuloplasty can prevent acute ischemic mitral regurgitation, but it also abolishes normal mitral annular and posterior leaflet dynamics. Ring annuloplasty, and other similar techniques, can lead to the deterioration of the performance of the mitral valve, including a loss of annular flexibility and the creation of a transvalvular gradient. This type of technique modifies or alters the normal function of the mitral valve. SLAC, on the other hand, can be implemented to preserve the physiologic dynamics of the mitral valve and its leaflets. Furthermore, SLAC can help to maintain the physiologic mitral annular morphology for proper function.
A recent study focused on the use of a conventional SLAC implementation to treat acute ischemic mitral regurgitation in animal hearts, illustrated the potential advantages offered by SLAC techniques. Timek T A et al., J Thorac Cardiovasc Surg., 2002 May; 123(5):881-8. The results of the study illustrated an average of a 22% (+/−10%) reduction in mitral annular septal-lateral dimension. This study concluded that this reduction in dimension reduced the acute ischemic mitral regurgitation while allowing near-normal mitral annular and posterior leaflet dynamic motion. Furthermore the study postulated that SLAC may represent a simple method for the surgical treatment of ischemic mitral regurgitation, either as an adjunctive technique or alone, which helps preserve physiologic annular and leaflet function.
Another conventional SLAC technique is disclosed in U.S. Patent Publication No. 2005/0143811 to Realyvasquez (“'811 Publication”). The '811 Publication discloses the implementation of SLAC using percutaneous deployment. FIG. 3 provides an illustration of the conventional device used to implement the SLAC technique disclosed in the '811 Publication. The device 50 shown in FIG. 3, is described in the '811 Publication as being delivered using a percutaneous intravascular catheter through the inter-atrial septum. Once the device is delivered, the two wired stents 52 are deployed and allowed to expand. The anterior portion of the stent 52 is attached to the annulus temporarily with the tines anchored to the wire. The posterior portion is anchored to the posterior annulus with similar tines. Once the stent is in proper position, the wires are re-enforced to their position with transvascular delivered fasteners to the posterior and anterior annular attachment points.
The device 50 disclosed in the '811 Publication includes a ratchet mechanism 60. This ratchet mechanism can be activated by the catheter that delivered the device 50. The '811 Publication describes that the catheter attached to ratchet mechanism 60 is turned in a counter clockwise direction, activating the ratchet mechanism 60. The rotation of the ratchet mechanism 60 operates to move the two wired stents 52 toward the center of the device 50. The '811 Publication discloses that the reduction in the distance between two wired stents 42 attached to the anterior annulus and the posterior annulus will serve to achieve the effect of septal-lateral annular cinching.
While the devices of the prior art are suitable for their intended purposes, they suffer from many drawbacks and fail to meet the demands of interventional cardiologists, cardiovascular surgeons, and the patients on whom they operate. Significantly, a need still exists for a minimally invasive device and associated technique to correct a deficient heart valve. More particularly, a need exists for a minimally invasive device and associated technique to restrict the septal-lateral diameter of an atrioventricular valve. Furthermore, the minimally invasive device and associated technique must be capable of implementation on a beating heart. It is highly desired to have a device capable of restricting the septal-lateral diameter of an atrioventricular valve which can be implemented in a variety of methods, including thoracoscopically and percutaneously.
Therefore, it would be advantageous to provide an apparatus and method for improving valve competence.
Additionally, it would be advantageous to provide an apparatus and method for restricting the dimension of a heart valve.
Additionally, it would be advantageous to provide an apparatus and method for correcting mitral valve regurgitation by restricting the diameter of a heart valve in a beating heart.
Additionally, it would be advantageous to provide an apparatus and method for restricting the diameter of a valve of a beating heart capable of being implemented in a minimally invasive manner.
Additionally, it would be advantageous to provide an apparatus delivered with a long arm or steerable needle from outside the heart for restricting the diameter of a valve of a beating heart.
Additionally, it would be advantageous to provide an apparatus capable of incrementally decreasing the septal-lateral diameter of an atrioventricular valve of a beating heart.
Additionally, it would be advantageous to provide an apparatus capable of decreasing the diameter of a heart valve in increments over an extended period of time.
Additionally, it would be advantageous to provide a method of reducing the dimension of a heart valve that enables a surgeon to easily access components used in an earlier surgery to later further restrict the dimension of the heart valve.
Additionally, it would be advantageous to provide a method of reducing the dimension of a heart valve that allows repeat reductions over an extended period of time.
Additionally, it would be advantageous to provide an apparatus and method for improving the morphology of beating heart valve without altering the physiologic dynamics of the heart valve.